Regular ArticleIncreased Sensitivity of Mitochondrial Respiration to Inhibition by Nitric Oxide in Cardiac Hypertrophy☆
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Cited by (55)
Mitochondria and Nitric Oxide
2017, Nitric Oxide: Biology and Pathobiology: Third EditionReactive Species and Mechanisms of Cell Injury
2014, Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease MechanismsCross talk between mitochondria and NADPH oxidases
2011, Free Radical Biology and MedicineCitation Excerpt :Mitochondrial membranes, proteins, and DNA (mtDNA) are particularly sensitive to oxidative damage [58,59]. ROS modify mitochondrial proteins, leading to their inactivation, as in the case of SOD2 and aconitase, or alter their function, as occurs with cytochrome c[60–62]. Superoxide reacts with 4Fe–4S clusters of complex I, complex II, and aconitase, resulting in the release of Fe3+ and altered protein function [16].
Loss of interstitial collagen causes structural and functional alterations of cardiomyocyte subsarcolemmal mitochondria in acute volume overload
2011, Journal of Molecular and Cellular CardiologyCitation Excerpt :Fluorescence was detected with the excitation at 460-500 nm and emission at 512-542 nm. Heart subsarcolemmal mitochondria (SSM) were isolated from LV tissue (70 mg) as previously described in our laboratory [16]. The pellet resulting from the centrifugation of LV homogenate at 1000xg for 5 minutes (4 °C) was considered to contain the intermyofibrillar mitochondria (IFM) and was divided into two aliquots: one was mixed with 25 mg/ml Nagarse (Sigma) solution in the isolation buffer for 5 minutes followed by the incubation with 2.5% BSA for 4 minutes and centrifugation at 1000xg for 4 min.
Characterization of short range DNA looping in endotoxin-mediated transcription of the murine inducible nitric-oxide synthase (iNOS) gene
2008, Journal of Biological Chemistry
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Please address all correspondence to: Peter G. Anderson, DVM PhD, Department of Pathology, University of Alabama at Birmingham, Volker Hall Rm. G046A, 1670 University Boulevard, Birmingham, AL 35294-0019. Tel: 205 934 2414. Fax: 205 934 1775. E-mail: [email protected]